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1 Obstetrics and Gynecology, University of Iowa, Iowa City, Iowa, United States
2 Internal Medicine, University of Iowa, Iowa City, Iowa, United States
3 Internal Medicine, University of Iowa, Iowa City, Iowa, United States; Physiology and Biophysics, University of Iowa, Iowa City, Iowa, United States
4 Internal Medicine, University of Iowa, Iowa City, Iowa, United States; VA Medical Center, Iowa City, Iowa, United States
* To whom correspondence should be addressed. E-mail: baoli-yang{at}uiowa.edu.
The present studies were designed to determine if mice heterozygous for
deletion of 
-ENaC exhibited defects in Na+/K+ transport and blood pressure regulation.
In response to an acute KCl infusion +/- mice developed higher serum [K+] and excreted
only 40% of the K+ excreted by +/+ mice. After 6 days on a low (0.01%) Na+ diet, the
cumulative Na+ excretion from day 3-6 was greater for +/- mice. This low Na+ diet
caused higher serum [K+] and lower K+ excretion rates in +/- mice than in +/+ mice, but
the rectal potential differences were not different. Analyses of mRNA from mice on this
diet showed the expected ~50% reduction of -ENaC in kidney and colon of +/- mice.
Unexpectedly, the level of 
-ENaC mRNA was similarly reduced. NHE3 mRNA was
~30% higher in +/- mice while mRNA of the Na/K/2Cl cotransporter was not different.
Also unexpectedly, the amount of -ENaC proteins was similar in both groups of mice
but there was a reduction of one form of -ENaC in +/- mice. These experiments
demonstrate that mice heterozygous for -ENaC have a small but detectable defect in
their ability to conserve Na+ and a more readily apparent defect in the ability to secrete
K+.
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